(a) Field of the Invention
A fusion protein including N-terminal domain of a fusion partner at N-terminal and C-terminal domain of RET protein at C-terminal, a fusion gene encoding the fusion protein, and a use of the fusion protein or the fusion gene as a diagnosing marker for a cancer, are provided.
(b) Description of the Related Art
Lung cancer remains a leading cause of mortality in cancer, with around 1.38 million deaths worldwide annually. With conventional chemotherapeutic regimen, the median survival time for lung cancer patients in advanced stages is less than one year from diagnosis. Tobacco smoking is known to be the major risk factor of lung cancer in Western countries, where 85% to 90% of all lung cancers were attributed to smoking. However, approximately 25% of lung cancer patients worldwide are ‘never-smokers’. Data from many Asian countries have shown that ‘never-smokers’ constitute 30-40% of non-small-cell lung cancer (NSCLC), which accounts for ˜80% of lung cancer cases. In NSCLC, a dominant histological type is adenocarcinoma (˜70%).
Lung cancer of never-smokers tends to be driven by single somatic mutation events, rather than global genetic and epigenetic changes. A subset of somatic mutations has been reported in NSCLC in the past few years, such as EGFR, KRAS and ALK genes (which are conventionally called as ‘the triple-markers’). Mutations in the tyrosine kinase domain of EGFR, which are associated preferentially with NSCLC of non-smokers and Asians, are sensitive to EGFR targeted therapy, such as Gefitinib. Missense mutations in KRAS are common in the lung adenocarcinomas of smokers, and induce resistance to EGFR inhibitors.
Although several genetic mutations have been reported, a large proportion of lung cancer patients have been observed to have none of them in their cancer genome. More than 40% of NSCLC appear to be driven by unknown genetic events. Therefore, it is needed to find more effective genetic markers for lung cancer.